Abstract

Objective: The present study was designed to investigate the possible molecular mechanisms of apoptosis in osteosarcoma induced by paclitaxel. Study design: Cell viability was detected in human osteosarcoma cell line HOS-732 treated with paclitaxel at different concentrations. The apoptosis and reactive oxygen species (ROS) production rates were determined by flow cytometry. COX-2 expression at mRNA and protein levels in osteosarcoma tissues were measured by quantitative real time polymerase chain reaction (RT-PCR) and Western blotting. Results: Paclitaxel can obviously inhibit the proliferation of HOS-732 cells in a dose-dependent manner. The production of ROS in HOS-732 cells was remarkably increased with the increasing concentration of paclitaxel. Moreover, paclitaxel can significantly inhibit the expression of COX-2 at mRNA and protein levels in rat osteosarcoma tissue. Furthermore, the inhibitory effects of paclitaxel on COX-2 expression at mRNA and protein levels were dose-related. Conclusion: Paclitaxel treatment can induce the apoptosis and increase the production of ROS in HOS-732 cells. Moreover, paclitaxel can decrease the expression of COX-2 in a dose-dependent manner. These findings suggested that paclitaxel-induced apoptosis in osteosarcoma could be ascribed to the increased production of ROS and the reduction of COX-2 expression.